Atorvastatin in stable angina patients lowers CCL2 and ICAM1 expression: Pleiotropic evidence from plasma mRNA analyses

6533b82efe1ef96bd1293c58

RESEARCH PRODUCT

Atorvastatin in stable angina patients lowers CCL2 and ICAM1 expression: Pleiotropic evidence from plasma mRNA analyses

Darja Stojanovic Ljubomir Sormaz Andrej Artenjak Katja Lakota Janja Marc Snezana Uletilovic Rizzo Manfredi Darko Cerne Bosa Mirjanic-azaric Snezna Sodin-semrl

subject

Male medicine.medical_specialty Chemokine Statin medicine.drug_class Atorvastatin Clinical Biochemistry Gene Expression Drug Administration Schedule In vivo Internal medicine Gene expression Atorvastatin medicine Humans Pyrroles Angina Stable RNA Messenger Serum amyloid A Chemokine CCL2 Aged biology Anticholesteremic Agents Atorvastatin CCL2 ICAM1 Interventional trial mRNA in plasma Pleiotropic effects C-reactive protein Cholesterol LDL General Medicine Middle Aged Intercellular Adhesion Molecule-1 Endocrinology Heptanoic Acids HMG-CoA reductase biology.protein Female lipids (amino acids peptides and proteins)medicine.drug

description

Objective: Statin pleiotropy is still an evolving concept, and the lack of clarity on this subject is due at least in part to the lack of a definitive biomarker for statin pleiotropy. Using plasma mRNA analysis as a novel research tool for the non-invasive in vivo assessment of gene expression in vascular beds, we hypothesised that atorvastatin lowers the plasmamRNA level from statin pleiotropy-target genes, and the reduction is independent of the reduction of low-density lipoprotein cholesterol (LDL-C). Design and methods: Forty-four patients with stable angina received atorvastatin therapy (20 mg/day, 10 weeks). Plasma chemokine (C-C motif) ligand 2 (CCL2) and intercellular adhesion molecule-1 (ICAM1) mRNA levels and their protein concentrations (MCP-1, sICAM-1) were analysed before and after the treatment. Plasma vascular adhesion molecule-1 (sVCAM-1) concentrations were also analysed. Results: Atorvastatin lowered plasma mRNA levels (CCL2: −31.76%, p = 0.037; ICAM1: −34.09%, p b 0.001) and MCP-1 protein concentration (−18.88%, p = 0.008) but did not lower sICAM-1 and sVCAM-1 protein concentrations, and the decreases appeared to be independent from the lowering of LDL-C. The plasma mRNA levels correlated with their protein concentrations following statin treatment only. Conclusion: Our results significantly strengthen the clinical evidence in support of statin pleiotropy. Furthermore, this unique simultaneous measurement of plasma mRNAs and their protein concentrations offers an advanced non-invasive in vivo assessment of the circulation pathology

year	journal	country	edition	language
2013-10-01	Clinical Biochemistry

https://doi.org/10.1016/j.clinbiochem.2013.06.006